الفهرس 
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Abstract
English summary
Recent studies have demonstrated that miRNA can regulate vascular inflammation, endothelial homeostasis, and angiogenesis. In particular, miR-126 has been shown to be involved in vascular dysfunction and inflammation. MiR-126 is highly enriched in ECs and endothelial apoptotic bodies and governs the maintenance of vascular integrity and angiogenesis (Fish et al,. 2008).
Moreover, miR-126 can facilitate vascular endothelial growth factor signaling pathway and modify vascular inflammation by suppressing leukocyte adhesion to ECs. MiR-126 regulates the expression of adhesion molecules in inflammatory ECs as well as inflammation response in ECs mediated by and angiotensin α . Another study revealed that miR-126 and angiotensin α type 1 receptor (AT1R) are co-expressed in ECs and vascular smooth-muscle cells and their expression is negatively correlated with the expression of the endogenous AT1R . A silent polymorphism (+1166 A/C) in the human AT1R has been shown to be associated with cardiovascular disease (CVD), which might be mediated by enhanced AT1R activity . Therefore, miR-126 might be responsible for endothelial activation and increased CVD risk in ESRD patients . (Zernecke et al,. 2009).
Recent studies have revealed that miRNAs previously identified in specific cells can also be detected in the circulation. study have shown that circulating levels of total and specific miRNAs were increased in patients with severe chronic renal failure, with important implications for the use of circulating miRNAs as biomarkers in patients with renal impairment and for the pathogenesis of uremia. In the present study, we measured the expression of miR-126, which were significantly increased in ESRD patients..( Amabile et al,. 2012) . Our data suggested that miR-126 might be useful predictive tools in ESRD; however, these results should be validated in a large clinical population, in which comparisons with standard risk factors could be made.